Diabetes Flashcards

1
Q

How does glucose get into a cell

3 points

A

Insulin binds to receptor

activates GLUT4 transporter.

Glucose into cell via ACTIVE TRANSPORT

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2
Q

On what cells are GLUT4 receptors found?

Or…

What cells require insulin for them uptake of glucose?

A

Skeletal muscle

Adipose

Liver

The rest of the cells don’t need insulin to take on glucose.. e.g. neurones

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3
Q

Define diabetes

T1DM

T2DM
1
2
3

A

Diabetes:
An endocrine disorder characterised by inadequate insulin production or supply.

T1DM;
an auto immune where the body attacks the beta cells in the pancreas, resulting in inadequate insulin production.

T2DM;

  1. Insulin receptor depletion as a result of increased sugars for a long time, sedentary lifestyle, excess adipose.
  2. Insulin resistance: less effective binding of insulin to cell receptor. Cells become less sensitive.
  3. The body starts to produce MORE INSULIN, beta cells become hypertrophic and increase in numbers. They over work and begin to atrophy > decreasing insulin production and increasing BSL.
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4
Q

Define insulin

How does insulin work

Promotes

Inhibits

A

Insulin: produced by the beta cells of the islets of langerhans in the pancreas.

Insulin lowers the bsl- binds to GLUT4 receptors and triggers the active transport of glucose into cells.

Inhibits:
Glycogenolysis
Gluconeogenesis
Lipolysis

Promotes:
Glycogenesis

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5
Q

Define glucagon

How does glucagon work?

Promotes

Inhibits

A

Glucagon is produced by the alpha cells in the pancreas.

Glucagon increases the bsl- works by activating the breakdown glycogen stores.

Promotes:
Gluconeogenesis
Glycogenolysis

Inhibits:
Glycogenesis

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6
Q

Define:

Glycogenolysis

Gluconeogenesis

Lipolysis

Glycogenesis

A

Glycogenolysis: the breakdown of glycogen to glucose

Gluconeogenesis: the formation of new glucose from non carb sources such as proteins.

Lipolysis: breakdown of fatty acids to glucose and keystones.

Glycogenesis: the formation and storage of glucose as glycogen

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7
Q

Signs and symptoms of diabetes

T1DM

T2DM May also have…

A
Increased bsl
Hypotension due to dehydration
Tachycardia
Polyuria (urine) > water follows glucose
Polydipsia (drinking) > dehydration - **but also cellular dehydration**
Headache
N&V
Decreased GCS
Blurred vision

T2DM
Polyphagia (eating) > decreased metabolism - greater need for energy

*eating more and losing weight due to effects of glucagon

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8
Q

What follows sign and symptoms of T1DM? 3 letters

Define.

2 parts.

A

Diabetic keto acidosis DKA

Pt. 1-
Begins with:
1. Insulin cannot inhibit fatty acid breakdown.
2. Lipolysis. The breakdown of fatty acids, producing ketone bodies.
…Acetate is the main keystone that smells fruity.
3. An anion gap is produced causing acidosis.
4. Potassium leaves cells - Increased serum potassium. - hyperkalaemia

Pt. 2-

  1. No insulin means increased bsl.
  2. Increased osmotic pressure draws fluid from cells - polyuria - water follows glucose.
  3. Full body potassium depletion.
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9
Q

Why don’t we give insulin to DKA

A

Because potassium will rush into cells and cause HYPERkalaemic arrhythmias.

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10
Q

What follows signs and symptoms of T2DM?

What don’t they get and why?

What do they get and why?

A

Type 2 don’t get DKA.
There is enough insulin to inhibit lipolysis.

They do get HONK- HHS
Hyper osmolar non ketoacidosis
Hyper osmolar hyperglycaemic syndrome

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11
Q

What is HONK

Define acronym

5 steps. Leading to shock

A

Hyper-osmolar non-ketone-acidosis
Or
Hyperosmolar hyperglycaemic syndrome.

  1. There is enough insulin to inhibit lipolysis but not enough to keep cells full of glucose.
  2. Increase bsl = increases osmolality
  3. Poly Dipsia, Uria, Phagia
  4. Dehydration
  5. Shock via fluid loss - not acidosis.
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